ArticleThe Prostate2009
Effects of the 5 alpha-reductase inhibitor dutasteride on gene expression in prostate cancer xenografts.
Article in The Prostate, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Cancer Chemoprevention: A Strategic Approach Using Phytochemicals.Frontiers in pharmacology · 2021Review
- Prostate cancer patients can benefit from 5-alpha-reductase inhibitor treatment: a meta-analysis.PeerJ · 2020Article
- Cell Size-Based Decision-Making of a Viral Gene Circuit.Cell reports · 2018Article
- 5α-reductase type 3 enzyme in benign and malignant prostate.The Prostate · 2014Article
- Novel interaction between the co-chaperone Cdc37 and Rho GTPase exchange factor Vav3 promotes androgen receptor activity and prostate cancer growth.The Journal of biological chemistry · 2013Article
- Article
- RhoA as a mediator of clinically relevant androgen action in prostate cancer cells.Molecular endocrinology (Baltimore, Md.) · 2012Article
- A novel nuclear role for the Vav3 nucleotide exchange factor in androgen receptor coactivation in prostate cancer.Oncogene · 2012Article
- Cross-talk between the androgen receptor and the liver X receptor: implications for cholesterol homeostasis.The Journal of biological chemistry · 2011Article
- Targeting 5α-reductase for prostate cancer prevention and treatment.Nature reviews. Urology · 2011Review
- Novel targets for prostate cancer chemoprevention.Endocrine-related cancer · 2010Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn the prostate, androgens play a crucial role in normal and cancerous growth; hence the androgenic pathway has become a target of therapeutic intervention. Dutasteride is a 5 alpha-reductase (5AR) inhibitor currently being evaluated both for chemoprevention and treatment of prostate cancer. Dutasteride inhibits both 5AR I and II enzymes, effectively blocking conversion of testosterone to dihydrotestosterone (DHT) in the prostate. This greatly reduces the amount of the active ligand DHT available for binding to the androgen receptor (AR) and stimulating proliferation, making this a good candidate for chemoprevention of prostate cancer. In this study, we sought to determine how dutasteride is functioning at the molecular level, using a prostate cancer xenograft model.
methodsAndrogen-responsive LuCaP 35 xenograft tumors were grown in Balb/c mice. Subcutaneously implanted time-release pellets were used for drug delivery. Microarray analysis was performed using the Affymetrix HG-U133Av2 platform to examine changes in gene expression in tumors following dutasteride treatment.
resultsDutasteride significantly reduced tumor growth in LuCaP 35 xenografts by affecting genes involved in apoptotic, cytoskeletal remodeling, and cell cycle pathways among others. Notably, genes in the Rho GTPase signaling pathway, shown to be important in androgen-deprivation conditions, were significantly up-regulated.
conclusionWe have identified multiple pathways outside of the androgenic pathway in prostate cancer xenografts affected by treatment with dutasteride. These findings provide insights into the function of dutasteride within the tumor microenvironment, potentially allowing for development of agents that can be used in combination with this drug to further enhance its effectiveness.
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Registered trials
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